Affiliations: [a] Student Research Committee, Urmia University of Medical Sciences, Urmia, Iran
| [b] Department of Clinical Pharmacy, School of Pharmacy, Urmia University of Medical Sciences, Urmia, Iran
| [c] Department of Pharmacology and Toxicology, School of Pharmacy, Urmia University of Medical Sciences, Urmia, Iran
Correspondence:
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Correspondence to: Dr. Morteza Ghasemnejad-Berenji, Assistant Professor, Department of Pharmacology and Toxicology, School of Pharmacy, Urmia University of Medical Sciences, PO Box: 5715799313, Urmia, Iran. Tel./Fax: +98 44 32754996; E-mails: morteza.ghasemnejad@yahoo.com and ghasemnejad.m@umsu.ac.ir. ORCID: orcid.org/0000-0001-5672-9202.
Abstract: In recent years, the association between the activity of platelets and risk of Alzheimer’s disease (AD) risk has been noticed in numerous studies. However, there in no investigations on the role of specific intracellular pathways to explain this connection. The phosphatidylinositol 3 kinase (PI3K)/AKT pathway is one of the main regulators of cell survival which regulates cellular responses to environmental changes. This pathway also regulates the activity of platelets, and its aberrant activity has been linked to platelet dysfunction in different pathologies. On the other hand, the PI3K/AKT pathway regulates amyloid-β (Aβ) production through regulation of amyloid-β protein precursor (AβPP), BACE-1, ADAMs, and γ-secretase. In addition, alterations in the activity of all of these factors in platelets has been shown in AD-related pathologies. Therefore, this paper aims to introduce the PI3K/AKT pathway as a molecular inducer of platelet dysfunction during aging and AD progression.
